Background Parkinson’s disease (PD) is a movement disorder. microRNA (miR)-133 expression is reduced in PD patients and in mice with a dopamine neuron deficiency. We aimed to identify the mechanism of miR-133a in apoptosis and autophagy in PD. Material/Methods The optimal concentration of MPP + (1-methyl-4-phenylpyridinium ion) was initially determined to construct a PD cell model. Gain-of function experiments were carried out to evaluate the role of miR-133a in PD. The levels of miR-133a, RAC1 (Ras-related C3 botulinum toxin substrate 1), apoptosis-related factors, and autophagy-related factors were detected after detection of cell proliferation, cell cycle, and apoptosis. Transmission electron microscopy was applied to observe autophagosomes, and immunofluorescence staining was performed to detect LC3 and further analyze the effect of miR-133a on autophagy in a PD cell model. Results Low miR-133a expression was detected in a cell model of MPP + -induced PD. After overexpressing miR-133a, cell proliferation increased, and apoptosis (cleaved caspase-3 and Bax levels decreased, while Bcl2 levels increased) and autophagy was inhibited (LC3II/I and Beclin-1 levels decreased, while p62 levels increased). MiR-133a targeted RAC1. RACY upregulation attenuated the inhibitory effects of miR-133a on PC12 cell apoptosis and autophagy. Conclusions Our data highlighted that miR-133a overexpression prevented apoptosis and autophagy in a cell model of MPP + -induced PD by inhibiting RAC1 expression.
This study was to explore the effect and mechanism of Let-7b nanocomposite on the expression of inflammatory factors in the cerebrospinal fluid (CSF) of purulent meningitis. 45 patients with purulent meningitis (PM) were selected as observation group (group A), and 38 patients with normal CSF without central nervous system diseases were selected as the control group (group B). The CSF of the two groups were collected to detect the inflammatory factors interleukin-8 (IL-8), macrophage inflammatory protein-1α (MIP-1α), matrix metalloproteinase 9 (MMP9), interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), and Let-7b level with the double antibody sandwich enzyme-linked immunosorbent assay (ELISA). The Let-7b nanocomposite was prepared, and its morphology, particle size, and Zeta potential were analyzed. In addition, the degradation kinetics, cytotoxicity, and phagocytic efficiency (PE) of Let-7b nanocapsules were detected. 36 healthy adult New Zealand (NZL) rabbits were randomly grouped into a control group (group C) (0.9% normal saline (NS)), a model group (Escherichia coli (E. coli) modeling, group D), and a test group (E. coli modeling + Let-7b nanocapsules, group E), with 12 rabbits in each group. The changes of inflammatory factors in CSF of the three groups were detected and compared. It was found that the expression levels of IL-8 and IL-1 β in the group A were much higher than those in the group B (P < 0.01), and the MMP9 and TNF-α levels in the group B were much lower in contrast to the group A (P < 0.001). The expression of Let-7b in the group A was lower obviously in contrast to the group B (P < 0.001). Let-7b nanocapsules were irregularly spherical, with an average particle size (APS) of 23.1 nm, a polydispersity index (PDI) of 0.232, and the Zeta potential of around +15 mV. Let-7b nanocapsules showed obvious polymer shell absorption peaks at 1,015 cm-1, 1,228 cm-1, and 1,547 cm-1. The IL-8 and IL-1β levels of the group D were greatly different from those in the other two groups (P < 0.01). The levels of TNF-α and MMP9 in the group D were greatly different in contrast to the group C (P < 0.001) and the group E (P < 0.01). It indicated that Let-7b nanocomposite could lower the expression levels of IL-8, IL-1β, MMP9, and TNF-α in the CSF of patients with purulent meningitis dramatically, which provides a reliable basis for immunotherapy of purulent meningitis with Let-7b.
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